M1 macrophage triggered by Mincle leads to a deterioration of acute kidney injury

Kidney Int. 2017 Mar;91(3):526-529. doi: 10.1016/j.kint.2016.11.026.

Abstract

In the early stage of acute kidney injury, M1 macrophages are proinflammatory and destructive. In this study, Lv et al. reveal that Mincle (macrophage-inducible C-type lectin, Clec4e) is expressed on M1 macrophages in acute kidney injury, and the kidney is protected in a murine model of cisplatin-induced renal injury by inhibiting Mincle expression on macrophages. Mincle expression is regulated by Toll-like receptor 4/nuclear factor κB signaling, and Mincle maintains the inflammatory phenotype through spleen tyrosine kinase signaling, leading to acute kidney injury.

Publication types

  • Comment

MeSH terms

  • Acute Kidney Injury
  • Animals
  • Lectins, C-Type
  • Macrophages*
  • Membrane Proteins*
  • Mice
  • Toll-Like Receptor 4

Substances

  • Lectins, C-Type
  • Membrane Proteins
  • Toll-Like Receptor 4